PUBLICATION
Calcium fluxes in dorsal forerunner cells antagonize {beta}-catenin and alter left-right patterning
- Authors
- Schneider, I., Houston, D.W., Rebagliati, M.R., and Slusarski, D.C.
- ID
- ZDB-PUB-071210-7
- Date
- 2008
- Source
- Development (Cambridge, England) 135(1): 75-84 (Journal)
- Registered Authors
- Rebagliati, Michael, Slusarski, Diane C.
- Keywords
- Calcium, Laterality, β-catenin, Zebrafish, Xenopus, Dorsal forerunner cells
- MeSH Terms
-
- Animals
- Body Patterning*
- Calcium/antagonists & inhibitors
- Calcium/metabolism*
- Calcium Signaling
- Cell Nucleus/metabolism
- Embryo, Nonmammalian/embryology
- Embryo, Nonmammalian/metabolism
- Gene Expression Regulation, Developmental
- Xenopus/embryology
- Xenopus/genetics
- Xenopus/metabolism
- Zebrafish/embryology
- Zebrafish/genetics
- Zebrafish/metabolism
- beta Catenin/antagonists & inhibitors*
- beta Catenin/metabolism*
- PubMed
- 18045845 Full text @ Development
Citation
Schneider, I., Houston, D.W., Rebagliati, M.R., and Slusarski, D.C. (2008) Calcium fluxes in dorsal forerunner cells antagonize {beta}-catenin and alter left-right patterning. Development (Cambridge, England). 135(1):75-84.
Abstract
Establishment of the left-right axis is essential for normal organ morphogenesis and function. Ca(2+) signaling and cilia function in the zebrafish Kuppfer's Vesicle (KV) have been implicated in laterality. Here we describe an endogenous Ca(2+) release event in the region of the KV precursors (dorsal forerunner cells, DFCs), prior to KV and cilia formation. Manipulation of Ca(2+) release to disrupt this early flux does not impact early DFC specification, but results in altered DFC migration or cohesion in the tailbud at somite stages. This leads to disruption of KV formation followed by bilateral expression of asymmetrical genes, and randomized organ laterality. We identify beta-catenin inhibition as a Ca(2+)-signaling target and demonstrate that localized loss of Ca(2+) within the DFC region or DFC-specific activation of beta-catenin is sufficient to alter laterality in zebrafish. We identify a previously unknown DFC-like cell population in Xenopus and demonstrate a similar Ca(2+)-sensitive stage. As in zebrafish, manipulation of Ca(2+) release results in ectopic nuclear beta-catenin and altered laterality. Overall, our data support a conserved early Ca(2+) requirement in DFC-like cell function in zebrafish and Xenopus.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping